Class IA antiarrhythmic + Na+ + K+ channel blocker; also potent CYP2D6 + P-glycoprotein inhibitor → classic raises-digoxin example. Dextrorotatory stereoisomer of quinine. Largely supplanted by safer antiarrhythmics.
Half-Life (t½)
PO: 10.34h, IV: 10.34h
Dosing Guidelines
PO: Typical 300 mg (Range: 200–600 mg)
Target Organ Systems
digestive
Interactions
Digoxin (major): Classic P-glycoprotein inhibition example. Rameis 1985 (PMID:3997300): quinidine prolonged digoxin t½ from 33 to 44 h, raised AUC ~2.65×, dropped renal CL from 150 to 79 mL/min (n=6 healthy crossover).
Dextromethorphan (major): CYP2D6 inhibition. Capon 1996 (PMID:8841152) verbatim: "quinidine increased the AUC in extensive metabolizers 43-fold". 6 EMs, single 30 mg DM + 50 mg quinidine 1 h later, 168 h sampling, crossover with placebo and quinidine-alone arms. Ki ≈ 1.5/(43-1) = 0.036 µM. Quinidine effectively converts EMs into PM-like DXM exposure — the basis for the DMQ (dextromethorphan/quinidine) combination product for pseudobulbar affect.
Propafenone (caution): CYP2D6 (5-hydroxylation). Funck-Brentano 1989 (PMID:2719900) verbatim: "quinidine increased mean steady-state plasma propafenone concentrations more than two fold, from 408 ± 351 to 1096 ± 644 ng ml-1 (P less than 0.001)". 7 EMs + 2 PMs on propafenone for VT; PMs unchanged. AUC 2.69×; Ki ≈ 0.888 µM. ECG/arrhythmia unchanged because 5-OH-propafenone is also active — interaction matters more for adverse effects than efficacy.
Desipramine (major): CYP2D6 inhibition (2-hydroxylation). Brøsen & Gram 1989 (PMID:2792169) verbatim: "During quinidine the total oral clearance of imipramine on average was reduced by 35%, and that of desipramine by 85%". 6 EMs of sparteine, single 100 mg PO desipramine ± quinidine 200 mg/d. 85% CL reduction maps algebraically to AUC ratio 1/(1-0.85) = 6.67×. Ki ≈ 1.5/5.67 = 0.265 µM. TCA narrow therapeutic index — anticholinergic + cardiac conduction risk with the 6-7× exposure rise; dose reduction needed.